Interleukin-2 receptor- -dependent endocytosis depends on biotin in Jurkat cells

Rodriguez-Melendez, Rocio, Gabriela Camporeale, Jacob B. Griffin, and Janos Zempleni. Interleukin-2 receptor-dependent endocytosis depends on biotin in Jurkat cells. Am J Physiol Cell Physiol 284: C415–C421, 2003. First published October 16, 2002; 10.1152/ajpcell.00365.2002.— Biotin has been credited with having beneficial effects on immune function despite observations that biotin supplementation causes decreased secretion of interleukin-2. Here this paradox was addressed by determining whether receptor-dependent internalization of interleukin-2 by immune cells depends on biotin. Theoretically, this would be consistent with both decreased net secretion of interleukin-2 by biotin-supplemented cells (causing increased endocytosis) and beneficial effects of biotin on immune function (causing increased receptor signaling). Jurkat cells were cultured in biotin-defined media (25, 250, or 10,000 pM). Secretion of interleukin-2 correlated negatively with biotin supply, but transcriptional activity of the interleukin-2 gene correlated positively with biotin supply, suggesting that decreased secretion of interleukin-2 by biotin-supplemented cells was not caused by decreased gene expression. Expression of the interleukin-2 receptorgene was greater at 10,000 pM than 25 pM biotin, mediating increased endocytosis of interleukin-2 in biotin-supplemented medium. Inhibition of endocytosis by genistein and overexpression of interleukin-2 receptorabolished the effect of biotin. These findings suggest that endocytosis of interleukin-2 depends on biotin.